Coarctation of the Aorta 

  • Author: P Syamasundar Rao; Chief Editor: Stuart Berger, MD   more...
 
Updated: Feb 1, 2012
 

Background

Coarctation of the aorta (CoA) is a relatively common defect that accounts for 5-8% of all congenital heart defects. Coarctation of the aorta may occur as an isolated defect or in association with various other lesions, most commonly bicuspid aortic valve and ventricular septal defect (VSD). The diagnosis of coarctation of the aorta may be missed unless an index of suspicion is maintained, and diagnosis is often delayed until the patient develops congestive heart failure (CHF), which is common in infants, or hypertension, which is common in older children. This article discusses the pathology, pathophysiology, clinical features, noninvasive and invasive evaluation, and therapy in patients with coarctation of the aorta.

Pathologic anatomy

Coarctation of the aorta may be defined as a constricted aortic segment that comprises localized medial thickening, with some infolding of the medial and superimposed neointimal tissue.[1] The localized constriction may form a shelflike structure with an eccentric opening or may be a membranous curtainlike structure with a central or eccentric opening. The coarctation may be discrete, or a long segment of the aorta may be narrowed; the former is more common.

In the past, coarctation of the aorta has been described as preductal (or infantile) type or postductal (or adult) type, depending on whether the coarctation segment is proximal or distal to the ductus arteriosus, respectively. However, a closer examination of the anatomy suggests that all coarctations are juxtaductal.

The classic coarctation of the aorta is located in the thoracic aorta distal to the origin of the left subclavian artery at about the level of the ductal structure. However, rarely, a coarcted segment is present in the lower thoracic or abdominal aorta. In such instances, the coarcted segment may be long and fusiform with irregular lumen; many consider these to be inflammatory or autoimmune in origin, and they may be variants of Takayasu arteritis.

Dilatation of the descending aorta immediately distal to the coarctation segment (poststenotic dilatation) is usually present. A jet lesion on the wall of the aorta distal to the coarctation site may also be present. Varying degrees of hypoplasia of the isthmus of the aorta (the portion of the aorta between the origin of the left subclavian artery and ductus arteriosus) are present in most patients with thoracic coarctation; this hypoplasia may be significant in symptomatic coarctation of the neonate and infant; in children and adults, the isthmus may have only mild narrowing. The transverse aortic arch (the arch between the origin of the right innominate artery and the left subclavian artery) is also hypoplastic in symptomatic neonates and infants. Collateral vessels that connect arteries from the upper part of the body to the vessels below the level of coarctation may be seen; these may be present as early as a few weeks to a few months of life.

The most commonly associated clinically significant defects include patent ductus arteriosus, VSD, and aortic stenosis. The earlier the infant presents, the more likely a significant associated defect is present. Bicuspid aortic valve may be seen in nearly two thirds of infants with coarctation of the aorta, whereas only 30% of those who present in childhood have such an anomaly.

Mitral valve anomalies, although less common than those of the aortic valve, are also associated with coarctation of the aorta. Sometimes, coarctation of the aorta is a complicating feature of a more complex cyanotic heart defect, such as transposition of the great arteries, Taussig-Bing anomaly, double-inlet left ventricle, tricuspid atresia with transposition of the great arteries, and hypoplastic left heart syndrome.

Aortic coarctation is extremely rare in patients with severe right ventricular outflow tract obstructions such as tetralogy of Fallot and pulmonary atresia with intact ventricular septum. Some patients with coarctation of the aorta may have cerebral aneurysms, predisposing them to cerebrovascular accidents with severe hypertension later in life. Coarctation of the aorta is the most common cardiac defect associated with Turner syndrome.

Pathogenesis

The exact mechanism by which aortic coarctation is produced is not clearly understood. The most commonly invoked hypotheses include hemodynamic and ectopic ductal tissue theories. In the hemodynamic theory, an abnormal preductal flow or abnormal angle between the ductus and aorta that increases right-to-left ductal flow and decreases isthmic flow potentiates development of coarctation. Postnatal spontaneous closure of the ductus arteriosus completes the development of aortic obstruction.[2, 3]

A high incidence of coarctation of the aorta in patients with congenital heart defects and decreased antegrade aortic flow in utero and virtual absence of CoA in patients with right heart obstructions lends credence to the hemodynamic theory. Abnormal extension of ductal tissue into the aorta (ectopic ductal tissue)[4, 5] has been postulated to create the coarctation shelf and, with ductal closure, development of aortic obstruction. This theory, however, does not explain the variable degrees of isthmus and aortic arch hypoplasia associated with coarctation of the aorta.

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Pathophysiology

Coarctation of the aorta imposes significant afterload on the left ventricle (LV), which results in increased wall stress and compensatory ventricular hypertrophy.

The afterload may be imposed acutely, as occurs following closure of the ductus arteriosus in neonates with severe coarctation. These infants may rapidly develop CHF and shock. Rapid constriction of the ductus arteriosus, producing sudden severe aortic obstruction, seems to be the most likely explanation. As the ductus (aortic end) constricts, the left ventricular afterload rapidly increases, with a resultant increase in left ventricular pressures (systolic and diastolic). This causes elevation of the left atrial pressure, which may open the foramen ovale, causing left-to-right shunt and dilatation of the right atrium and right ventricle. If the foramen ovale does not open, pulmonary venous pressures and pulmonary artery pressures increase, and right ventricular dilatation develops.

Cardiomegaly revealed by chest roentgenography and right ventricular hypertrophy seen on ECG and echocardiography are related to the indirect effects of rapid development of severe aortic obstruction.

LV afterload may also gradually increase, allowing children with less severe coarctation to develop arterial collateral vessels that partially bypass the aortic obstruction. These children may be asymptomatic until hypertension is detected or another complication develops.

The mechanism for development of hypertension is not clearly understood; mechanical obstruction and renin-angiotensin–mediated humoral mechanisms have been postulated.

The mechanical obstruction theory explains the increased blood pressure by postulating that a higher blood pressure is required to maintain flow through the coarcted segment and collateral vessels. The stroke volume, ejected into the limited aortic receptacle, produces a higher pressure proximal to coarctation. However, this theory does not explain the following:

  • The lack of relationship between the degree of elevation of blood pressure and the magnitude of obstruction
  • The increased peripheral vascular resistance distal to the site of obstruction
  • The delayed or lack of reduction of blood pressure immediately following relief of obstruction

The humoral theory postulates activation of the renin-angiotensin system secondary to reduction of renal blood flow and appears to explain most of the clinical features.[6, 7, 8] However, measurement of plasma renin activity in both animal models and human subjects did not show consistently elevated plasma renin levels in the early studies. The reasons for the inability to demonstrate elevation of renin levels may be related to inadequate measurement of salt intake, posture, extracellular fluid volume, and sympathetic influences on renin release. More recent studies demonstrated abnormalities in renin-angiotensin-aldosterone systems.[9] In addition, activation of central sympathetic nervous system may also be responsible for hypertension of aortic coarctation.[10]

Associated anomalies greatly influence pathophysiology.[11] VSD is also frequently present, and coarctation exacerbates the associated left-to-right shunt. Other levels of left heart obstruction (aortic stenosis, subaortic stenosis) may be present and may add to LV afterload.

Numerous neurohumoral changes occur with CHF.[12] Sympathetic nervous system activation occurs, resulting in increases in heart rate and blood pressure (BP). The renin-angiotensin system is activated in patients with CHF, particularly in coarctation of the aorta, in which lower-body BP and renal perfusion may be reduced. Activation of the renin-angiotensin system results in vasoconstriction, cell hypertrophy, and the release of aldosterone. The role of the renin-angiotensin system in CHF and the use of drugs to modulate this system are an intense area of research. Unlike most cases of CHF, coarctation of the aorta is more complex because precoarctation and postcoarctation hemodynamics are quite different.

Drugs typically used to treat patients with CHF, such as ACE inhibitors and, more recently, angiotensin II antagonists, may have adverse effects in patients with coarctation of the aorta. Attempts to achieve a normal precoarctation BP with these drugs may result in inadequate lower-body perfusion and may precipitate renal failure.

Vasopressin is also increased in heart failure, although its major stimulus for release is angiotensin II. Vasopressin affects free water retention and may result in hyponatremia. The vasoconstrictive properties of vasopressin may further elevate BP in coarctation.

Other substances, such as human brain natriuretic peptide (BNP), an endothelin, may be activated by CHF, although their specific role in coarctation has not been studied.

An additional cause of coarctation of the aorta is trauma that results in aortic dissection. Compromise of the true lumen of the aorta can result in the clinical picture of coarctation with reduced lower-extremity pulses. Urgent intervention is required in this circumstance.

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Epidemiology

Frequency

United States

Coarctation of the aorta is a common defect and occurs in 6-8% of patients with congenital heart disease.[13, 14] However, coarctation may be found more frequently in infants who present with symptoms prior to age one year.[11]

International

The prevalence of coarctation of the aorta appears to be lower (< 2%) in Asian countries than in European and North American countries.[15]

Mortality/Morbidity

Past autopsy studies suggest that the mortality rate in patients in whom coarctation of the aorta is not surgically repaired is 90% by age 50 years, with a mean age of 35 years.[16] In the current era, coarctation of the aorta mortality is often determined by patient age, patient size, and associated major cardiovascular anomalies.

Associated problems that may contribute to death or morbidity include hypertension, intracranial hemorrhage, aortic rupture or dissection, endocarditis, and CHF.

Race

No definitive racial differences have been documented in coarctation of the aorta, although some authors have suggested that coarctation of the aorta is less common in Asians.[15]

Sex

The male-to-female ratio is 2:1, although this ratio is not valid in abdominal coarctation of the aorta, in which this rare lesion predominantly affects females. The ratio of abdominal-to-thoracic coarctation is approximately 1:1000. The male preponderance observed in older patients is not seen in infants with coarctation of the aorta.

Age

Generally, patients with coarctation of the aorta present early in life with CHF or later in life with hypertension. Studies continue to document that coarctation of the aorta is often missed in the first year of life,[17, 18] and the median age of referral to a pediatric cardiologist in one study was 5 years. Among 2192 patients reported to the Pediatric Cardiac Care Consortium from 1985-1993, 1337 were infants, 824 were children, and 31 were adults.[19]

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Contributor Information and Disclosures
Author

P Syamasundar Rao  MD, Professor of Pediatrics, Division of Cardiology, University of Texas Medical School at Houston; Director, Division of Pediatric Cardiology, Children's Memorial Hermann Hospital; Professor of Pediatrics, MD Anderson Cancer Center, University of Texas

P Syamasundar Rao is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Medical Association, American Pediatric Society, Medical Association of Georgia, Society for Cardiac Angiography and Interventions, Society for Pediatric Research, Southern Society for Pediatric Research, and Western Society for Pediatric Research

Disclosure: Nothing to disclose.

Coauthor(s)

Paul M Seib, MD  Associate Professor of Pediatrics, University of Arkansas for Medical Sciences; Medical Director, Cardiac Catheterization Laboratory, Co-Medical Director, Cardiovascular Intensive Care Unit, Arkansas Children's Hospital

Paul M Seib, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Arkansas Medical Society, International Society for Heart and Lung Transplantation, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Specialty Editor Board

Juan Carlos Alejos, MD  Clinical Professor, Department of Pediatrics, Division of Cardiology, University of California, Los Angeles, David Geffen School of Medicine

Juan Carlos Alejos, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Medical Association, and International Society for Heart and Lung Transplantation

Disclosure: Actelion Honoraria Speaking and teaching

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Julian M Stewart, MD, PhD  Associate Chairman of Pediatrics, Director, Center for Hypotension, Westchester Medical Center; Professor of Pediatrics and Physiology, New York Medical College

Julian M Stewart, MD, PhD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Gilbert Z Herzberg, MD  Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College; Consulting Staff, Department of Pediatrics, Sound Shore Medical Center

Gilbert Z Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD  Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital of Wisconsin

Stuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

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Aortic coarctation visualized by aortic angiography.
Aortic coarctation visualized by MR imaging.
 
 
 
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